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1 The Liggins Institute, University of Auckland, Auckland, New Zealand
* To whom correspondence should be addressed. E-mail: l.bennet{at}auckland.ac.nz.
Renal impairment is common in preterm infants, often after exposure to hypoxia / asphyxia or other circulatory disturbances. We examined the hypothesis that this association is mediated by reduced renal blood flow (RBF), using a model of asphyxia induced by complete umbilical cord occlusion for 25 min (n=13) or sham occlusion (n=6) in chronically instrumented preterm fetal sheep (104 days, term is 147 days). During asphyxia there was a significant fall in RBF and urine output (UO). After asphyxia, RBF transiently recovered, followed within 30 min by a secondary period of hypoperfusion (P<0.05). This was mediated by increased renal vascular resistance (RVR, P<0.05); arterial blood pressure was mildly increased in the first 24 h (P<0.05). RBF relatively normalised between 3 to 24 h, but hypoperfusion developed again from 24 to 60 h (P<0.05, ANCOVA). UO significantly increased, to a peak of 249 % of baseline between 3 and 12 h (P<0.05), with increased fractional excretion of sodium, peak 10.5±1.4 vs. 2.6±0.6 % (P<0.001). Creatinine clearance returned to normal after 2 h; there was a transient reduction at 48 h to 0.32±0.02 ml/min/g (vs. 0.45±0.04, P<0.05) corresponding with the time of maximal depression of RBF. No renal injury was seen on histological examination at 72 h. In conclusion, severe asphyxia in the preterm fetus was associated with evolving renal tubular dysfunction, as shown by transient polyuria and natriuresis. Despite a prolonged increase in renal vascular resistance there was only a modest effect on glomerular function.
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